槲皮素预处理通过抑制ERK/NF-κB信号通路减轻肝缺血再灌注诱导的细胞凋亡和自噬。
Quercetin Pretreatment Attenuates Hepatic Ischemia Reperfusion-Induced Apoptosis and Autophagy by Inhibiting ERK/NF-B Pathway.
作者信息
Wu Liwei, Zhang Qinghui, Dai Weiqi, Li Sainan, Feng Jiao, Li Jingjing, Liu Tong, Xu Shizan, Wang Wenwen, Lu Xiya, Yu Qiang, Chen Kan, Xia Yujing, Lu Jie, Zhou Yingqun, Fan Xiaoming, Guo Chuanyong
机构信息
Department of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Department of Clinical Laboratory, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu 215300, China.
出版信息
Gastroenterol Res Pract. 2017;2017:9724217. doi: 10.1155/2017/9724217. Epub 2017 Oct 16.
BACKGROUND
Hepatic ischemia reperfusion (IR) injury is a common phenomenon in transplantation or trauma. The aim of the present study was to determine the protective effect of quercetin (QE) on hepatic IR injury via the ERK/NF-B pathway.
METHODS
Mice were randomized into the sham, IR, QE100 + IR, and QE200 + IR groups. Quercetin was administered intragastrically daily at two doses (100 mg/kg and 200 mg/kg) for 5 days prior to IR injury. The expression levels of liver enzymes, inflammatory cytokines, and other marker proteins were determined at 2, 8, and 24 hours after IR. And they were compared among these groups.
RESULTS
Compared with the IR group, the treatment of QE reduced the release of cytokines, leading to inhibition of apoptosis and autophagy via downregulation of the ERK/NF-B pathway in this model of hepatic IR injury.
CONCLUSION
Apoptosis and autophagy caused by hepatic IR injury were inhibited by QE following a reduction in the release of inflammatory cytokines, and the relationship between the two may be associated with inactivation of the ERK/NF-B pathway.
背景
肝缺血再灌注（IR）损伤是移植或创伤中常见的现象。本研究的目的是通过ERK/NF-κB途径确定槲皮素（QE）对肝IR损伤的保护作用。
方法
将小鼠随机分为假手术组、IR组、QE100 + IR组和QE200 + IR组。在IR损伤前5天，每天以两种剂量（100 mg/kg和200 mg/kg）灌胃给予槲皮素。在IR后2、8和24小时测定肝酶、炎性细胞因子和其他标志物蛋白的表达水平，并在这些组之间进行比较。
结果
与IR组相比，在该肝IR损伤模型中，QE处理减少了细胞因子的释放，通过下调ERK/NF-κB途径导致细胞凋亡和自噬的抑制。
结论
肝IR损伤引起的细胞凋亡和自噬在炎性细胞因子释放减少后被QE抑制，二者之间的关系可能与ERK/NF-κB途径的失活有关。
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